BOTULISM

This is a highly fatal motor paralysis caused by

ingestion of a neurotoxin produced by a
Gram-positive, spore forming anaerobic
bacterium, Clostridium botulinum.
Seven antigenically distinct toxin types (A-G),
some with subtypes, have been identified.
Farm animal disease is
produced primarily
by types B, C and D.
 Epidemiology
The vegetative form of C. botulinum is commonly found in
the intestinal tract of herbivores and faeces &
contaminate the environment.
spores ; highly resistant to environmental conditions.
C. botulinum ; proliferate only in decomposing animal
carcasses or sometimes plant materials.
Carrion animals may spread the organisms from one area to
another. Pica caused by deficiency of protein or starvation
may force animals to crave on infected carrion or
decomposing plant materials and subsequent ingestion of
lethal doses of the toxin.
Warm and wet conditions are favourable for the
proliferation of C botulinum and toxin production.
 Source of infection
forage botulism; ingestion of preformed toxin
Big bale silage is a particular risk. Which fail to
achieve a stable low pH, and the higher dry matter content
can also lead to a higher pH. Clostridial multiplication is
inhibited below pH 4.5.
carrion-associated botulism:
Direct carrion ingestion can occur where cattle subsist on a
phosphorusdeficient diet
wound botulism: less common source
Poultry manure and ensiled poultry
litter have caused outbreaks of botulism
when used as cattle feed
• Toxicoi nfectious botulism
This results when toxin is produced by
C. botulinum present in the intestine. The
disease is also called the 'shaker foal
syndrome'. young foals up to 8 months of age
with the highest prevalence in foals 3-8 weeks of
age
 Pathogenesis
Proteolytic enzymes present in the alimentary
tract digest the toxin so large doses needed
P/0 Intestinal wall systemic circ.
Presence of the toxin at the neuromuscular
junctions inhibits the secretion of
Acetylcholine flaccid paralysis
asphyxiation following paralysis of the
respiratory muscles & lead to death
 Clinical features
In initial stages, the acute disease is characterised by
stiffness of muscles, incoordination and excitability. The
listless and, the head is raised or lowered during walking or
may be held on one side. torticollis.
Lateral bending of the tail, arching of the back,
salivation, serous nasal discharges and frequent urination
also occur.
Abdominal respiration and flaccid paralysis are observed
in the terminal stages of the acute disease.
The chronic disease is characterised by ruminal and
intestinal stasis.
 Cattle and horses

Signs appear 3-17 days post exposture

Peracute : die without prior signs of illnes, No fever,
charcteristic flacid paralysis
Colic an initial sign in horses.
Subacute: Restlessness, incoordination, stumbling,
knuckling, and ataxia, inability to rise or to lift the head
Sternal recumbency with the head on the ground
not unlike the posture of a cow with parturient paresis
tongue becomes paralyzed and hangs from the mouth
• Ruminal movements depressed chronic cases
show restlessness and respiratory distress
followed by knuckling, stumbling, and
disinclination to rise.
• Anorexia and adipsia are important early signs
 Sheep
Sheep do not show the typical flaccid paralysis of other
species until the final stages of the disease.
Stiffness while walking, and incoordination and
some excitability in the early stages.
The head may be held on one side or bobbed (short
movement up and down) up and down while walking .
Lateral switching of the tail,
salivation, and serous nasal discharge .
In the terminal stages ,abdominal respiration, limb
paralysis, and rapid death.
 Pathological features
No specific pathological features are associated
with the disease
Perivascular haemorrhage in
the brain and
destruction of the Purkinje cells
may be evident in histological
sections.
 Diagnosis
Demonstration of large quantities of the toxin in
suspected feed or intestinal tracts of dead
animals is diagnostic.
Botulism resembles the paralytic form of rabies,
Plant poisoning, lead poisoning,
polioencephalomalacia ,hypocalcaemia,
hypomagnesaemia and louping ill
 Treatment and Control
• A hyperimmune serum given together with the antitoxin for 5 days
may result in recovery.
• Treatment is not effective in late stages of the disease.
• Good nursing and supportive intravenous or stomach tube feeding
• put on sternal recumbency to prevent bloat.
• Proper disposal of carcasses to avoid contamination of the
pastures
• A polyvalent toxoid containing type A, B, C
• and D strains is commercially available.
• Adminitered dose of 30 000 IU for a foal and 70 000 IU
• for adult horses